Critique of Georgi/Mercola/Ray Peat

[Peater]

This thread is making me hungry.

 

[Mr Joe]

Haha I am just playing along, of course they drank milk. But they also ate solid food, something a lot of men need to think about doing in this community.

Old testament times were much different than new testament times too. They were shepherding people. That verse I quoted was about spiritual maturity not about actual food.

you know sh*t gets real when people bring in jesus as a reference

hahaha I was just bringing Jesus because that's funny reading "InChristAlone" preaching VitA toxicity. Someone has to be wrong there. We always have the "you don't understand it's metaphorical" or "it was not the same time" jokers though...

 

[charlie]

Deuteronomy 32:14​

"Butter of the herd, and milk of the flock, with fat of lambs, rams of the breed of Bashan, and goats, with the finest of the wheat. Of the blood of the grape you drank wine."

Nahh... Come on bro don't make me think you believe Jesus wasn't drinking milk and eating butter !

There are people in the low A groups that drink a cup or so of milk for the natural lactoferrin. It needs to be not pasteurized though since the heat makes the milk more toxic by turning vA into more toxic forms. Also plenty of people still eat butter too. We are able to clear a certain amount of vA a day, each person being different depending on liver health status.

 

[haidut]

It takes months and sometimes years for the thyroid to recover from poison vA. All vitamin E does is shove the vA into the liver so it makes it look like things are better, while filling up the liver with more toxic vA. When I was at my worst eating the typical Peat diet, I too was able to get relief from vA for a short bit by taking vitamin E. All it was doing was suppressing the symptoms by getting it out of the blood temporarily.

The gold standard from vA testing is a liver biopsy. Studies back in the 50's showed a third of the people tested via biopsy were vA toxic. Imagine now how high that percentage is with all the glyphosate and added and supplemented vA going around now.

Let me ask you this, Georgi. Why are more and more people able to get off their thyroid hormones after doing the low vA and low toxin diet? Does that not make you raise an eyebrow? Should we not be trying to get people off hormones instead of chaining them up for life? I absolutely believe thyroid hormones can and should be used as a crutch until full liver function comes back online but taking it for life is not a health solution, it sounds like captivity to me.

Have you checked out this twitter thread below by Dr. Smith?

View: https://twitter.com/NutriDetect/status/1594364556050313216


And lastly, throwing all studies aside. Results is what should really matter in the end. Grant healed stage 4 kidney disease! And results on the level that are happening in the low vA and low toxin groups are nothing short of miraculous. We all know we can find a study to suit our bias. However, if you are on the wrong bias you are going to get disastrous results like has been in the Ray Peat groups. There are people in the low vA groups literally calling Peat a murderer now because of how bad his diet recommendations harmed them. I do not agree with that kind of sentiment but the feelings are real for these people. They, like myself, were hurt badly by the Ray Peat way. Georgi, you yourself have been overweight for most this journey, wake up brother! I have lost almost 50 pounds not even trying! I feast like a king! A healthy diet should not make you fat! A healthy diet should not give you fatty liver like it did me or ecstatichamster, a healthy diet should not melt your teeth like it did me and Ray Peat himself.

My lab back in Europe works with people with liver disease. Some of them had biopsies and the typical presentation is LOW for all fat-soluble vitamins, high on both raw PUFA as well as its perodixation byproducts, and high in iron/copper - i.e. pretty much what Peat said would happen when thyroid function is low and/or diet is crappy. I am not rejecting the theory of vitA toxicity, one has to keep an open mind. However, it is hard to accept that vitA toxicity won't show up blood or hair/nail tests if there is indeed toxicity. I don't know of any mechanism through which vitamin E somehow keeps vitamin A inside the liver, thus masking its presence and fooling the blood tests. There is no such function known for vitamin E nor there is a known mechanism through which it can keep vitA "imprisoned" in the liver. The carrier of vitA known as retinol binding protein (RBP) is made in the liver, and is completely independent of the tocopherol binding protein(s).

Retinol-binding protein - Wikipedia

en.wikipedia.org

So, if one is not making enough RBP (which would indeed result in vitA accumulation and toxicity) then liver dysfunction is already present and quite severe as the production of proteins such as albumin, globulin, vitamin carrier proteins, etc is probably the last liver function to fail, and such failure is a pretty severe sign that is an independent cause of disease or mortality, regardless of vitamin A intake.

Moreover, not sure how people would get this vitA toxicity since the food fortification in Western countries barely meets the RDA, which itself was based on keeping prisoners barely alive. Where is this massive flow of vitA coming from to poison people? It surely ain't the food, even the commercial/prepared one, which is fortified. In fact, about half of the world's population and 40%+ of the US population have deficient intake of vitamin A, and considering that metric is based on the woefully inadequate RDA value, the deficiency is probably even more wide spread and severe than the numbers suggest.

Are you getting enough vitamin A? Probably, but half of the world isn't

Scientists are genetically modifying crops like rice to get vitamin A into impoverished diets in southeast Asia and sub-Saharan Africa. NewsHour explains why this vitamin is so important, where you can get it and why you shouldn't eat polar bear liver.

www.pbs.org

Micronutrient Inadequacies in the US Population: an Overview

Contents Assessing Nutrient Intake US national dietary surveys Nutritional biomarkers Micronutrient Deficiencies and Inadequacies Shortfall Micronutrients Calcium Iron Magnesium Po

lpi.oregonstate.edu

"...Specifically, 94.3% of the US population do not meet the daily requirement for vitamin D, 88.5% for vitamin E, 52.2% for magnesium, 44.1% for calcium, 43.0% for vitamin A, and 38.9% for vitamin C. "

Now, synthetic retinoids (acitretin, etretinate, tretinoin, etc) are indeed very liver-toxic, as are some natural analogs/isomers of retinoic acid, but those are only rarely used (i.e. severe acne or blood cancers) and thus affect only a small portion of people. The natural retinol and retinoic acid(s) have been used in massive doses on people daily and not shown any serious (and especially, liver) toxicity.

Reports Of Vitamin A Toxicity Are Greatly Exaggerated

This is a human study and as you can see it used up to 500,000 IU vitamin A daily for months for acne treatment without any serious signs of toxicity. Most doctors will warn you that vitamin A will cause liver issues, but as you can see this was not the case here...

raypeatforum.com

Vitamin A (retinol) Is Not Toxic To The Liver In High Doses

As a follow up on my previous post, this study looks at toxicity of retinol acetate in doses exceeding 300,000 IU per day taken for months and in combination with a SERM (tamoxifen) which itself is quite estrogenic and as such is a proven liver burden. http://www.ncbi.nlm.nih.gov/pubmed/3218964

raypeatforum.com

To the contrary, some of the best new drugs for liver disease are either higher doses retinol (and its esters) or even synthetic retinoid acid agonists, though I'd be cautious with the latter until they have been in use for at least 2 decades so that their full toxicity profile is known. In fact, vitamin A is required for liver regeneration as well as prevention of liver fibrosis developing into cancer.

Vitamin A (retinol) reduces hepatic cancer incidence by 89%!

I know a lot of people here avoid taking vitamin A or do so at very low doses out of fear of liver toxicity. In theory, anything that is toxic to the liver would tend to cause hepatic carcinoma in the long run. However, in the case of vitamin A (retinol) not only there seems to be no liver...

raypeatforum.com

Retinoids in the Pathogenesis and Treatment of Liver Diseases

Vitamin A (VA), all-trans-retinol (ROL), and its analogs are collectively called retinoids. Acting through the retinoic acid receptors RARα, RARβ, and RARγ, all-trans-retinoic acid, an active metabolite of VA, is a potent regulator of numerous biological pathways, including embryonic and somatic...

www.mdpi.com

"...Many experiments have been performed to assess the effects of dietary vitamin A deficiency on liver functions. Adult, vitamin-A-deficient (VAD) rats showed hepatocyte vacuolization, a sign of steatosis, and mild inflammation in the liver [48]. In VAD rats, hepatic gluconeogenesis is decreased relative to that in vitamin-A-sufficient animals [49]. Moreover, a low level of retinoids in the liver at the time of carbon tetrachloride treatment greatly accelerated the process of liver fibrosis in rats [50]. This occurred concomitant with a selective loss of retinyl palmitate and a larger percentage of retinyl esters in the form of retinyl oleate and retinyl stearate. Furthermore, after common bile duct ligation, VAD rats displayed enhanced proliferation of bile duct epithelial cells [51]. Vitamin A is required for hepatocyte survival in a liver regeneration model partial hepatectomy (PHE) in rats [52]. Moreover, compared to wild-type mice, mice that lack lecithin:retinol acyltransferase (Lrat−/−) and thus are unable to store hepatic retinoids show delayed hepatic regeneration after partial hepatectomy [53]. These data indicate that a lack of hepatic retinoid hinders the survival and regeneration of hepatocytes after liver injury; however, the mechanisms by which low retinoids lead to defective hepatic regeneration were not identified in these studies."

"...The RARs α, β, and γ and the RXRs α, β, and γ are all expressed in the liver [54]. The critical functions of the RARs in the liver were strikingly shown by using transgenic mice in which an RAR-α-dominant negative construct, driven by the albumin promoter, was expressed selectively in hepatocytes [55,56]. This construct suppresses the functions of all three RARs, α, β, and γ. The liver-selective RARα-dominant-negative mice showed both microvesicular steatosis at 4 months of age and a decrease in mitochondrial β-oxidation of fatty acids. These mice had hepatocellular carcinoma and adenoma of the liver at one year. Notably, feeding these mice a high-RA diet reversed these biochemical abnormalities and reduced the development of liver tumors. Thus, loss of RA actions specifically in the liver led to steatohepatitis and liver tumors. Since all three RARs were affected in these experiments, it is not possible to determine the roles of each of the RARs in the prevention of steatohepatitis and liver tumors. Conversely, treatment of wild-type mice with exogenously added RA shifted lipid metabolism toward reduced lipogenesis and increased catabolism [57,58]. We will discuss the actions of retinoids in the inhibition of non-alcohol-associated liver disease and liver cancer in rodent models and in humans in more detail in Section 4 and Section 6."

"...Excessive free fatty acids in the liver are esterified into triglycerides that are stored as lipid droplets in hepatocytes, manifested as liver steatosis. De novo fatty acid synthesis converts non-lipid precursors into fatty acids, and de novo fatty acid synthesis can contribute almost 40% of intrahepatic triglycerides in subjects with NAFLD [80]. In mammalian cells, first, acetyl-CoA carboxylase converts acetyl-CoA to malonyl-CoA. Then fatty acid synthase (FASN), an enzyme containing multi-functional subunits with seven enzymatic activities: acetyl-CoA-ACP transacylase, malonyl-CoA-ACP transacylase, β-ketoacyl-ACP condensase, β-ketoacyl-ACP reductase, β-hydroxyacyl-ACP dehydratase, enoyl-ACP reductase, and palmitoyl-ACP thioesterase, initiates fatty acid synthesis using acetyl-CoA and malonyl-CoA [81]. The final product of FASN is palmitate, a saturated fatty acid. Fatty acids with longer chains and unsaturated fatty acids are produced from palmitate through different enzymes, i.e., elongases (ELOVLs) and desaturases [82,83]. Stearoyl-CoA desaturase 1 (SCD1) catalyzes the first desaturation reaction to produce the first double bond in palmitate and stearate [83]. Many lipid species, including triglycerides and phospholipids, are generated from saturated and unsaturated fatty acids.
Retinoic acid suppresses lipid biosynthesis in mouse liver, and RA decreases the mRNA levels of both SREBF and FASN, which are involved in de novo lipogenesis [57,84] (Figure 2). RA also reduces lipid accumulation and steatosis in the liver of NAFLD mouse models [85,86,87,88]."

Again, I am keeping an open mind and not rejecting this hypothesis, but I think we would need some more direct evidence before we can lay blame squarely at vitA as a cause of virtually all diseases, as Genreux claims. If you have some of those studies on vitA liver biopsies showing toxicity, please send some.

@ALS @Mr Joe

 

[Peater]

Appreciate the effort-post @haidut - interesting that you too do flag excess copper. Can retinol binding protein levels be tested, either through basic DIY methods (I don't know the correct term for this) or lab tests?

 

[haidut]

Appreciate the effort-post @haidut - interesting that you too do flag excess copper. Can retinol binding protein levels be tested, either through basic DIY methods (I don't know the correct term for this) or lab tests?

Yes, they can, but it requires a lot more tissue to be biopsied/collected and for most people the ethical/protocol requirements do not allow for that. It can be done at autopsy, but getting an approval to do such a study would take years. It is easier to test for simple molecules such as minerals, steroids, vitamins, etc than large peptides such as RBP. Now, if those peptides accumulate in hair/nails and are stable there, we may be able to test them, but it would be subject to the same requirements probably - i.e. we'd need a bigger hair/nail sample. However, it would still be more feasible and a lot less invasive than cutting small chunks from somebody's liver.

 

[Peater]

Yes, they can, but it requires a lot more tissue to be biopsied/collected and for most people the ethical/protocol requirements do not allow for that. It can be done at autopsy, but getting an approval to do such a study would take years. It is easier to test for simple molecules such as minerals, steroids, vitamins, etc than large peptides such as RBP. Now, if those peptides accumulate in hair/nails and are stable there, we may be able to test them, but it would be subject to the same requirements probably - i.e. we'd need a bigger hair/nail sample. However, it would still be more feasible and a lot less invasive than cutting small chunks from somebody's liver.

Thanks again, that makes sense. In theory, could the problem be low RBP somehow? (As well as possibly high iron and copper)

 

[haidut]

Thanks again, that makes sense. In theory, could the problem be low RBP somehow? (As well as possibly high iron and copper)

Liver damage caused by excess iron can certainly cause low RBP as well as low other proteins produced by the liver. Copper can also damage the liver if taken in pure form and in high amounts by a hypo person, since in a hypo person the production by liver of the copper-carrier protein ceruloplasmin would be low and copper will accumulate in the liver in unbound form -i.e. very reactive. That being said, with aging we tend to accumulate way more iron than copper, so the typical presentation is iron overload.

 

[Peater]

Liver damage caused by excess iron can certainly cause low RBP as well as low other proteins produced by the liver. Copper can also damage the liver if taken in pure form and in high amounts by a hypo person, since in a hypo person the production by liver of the copper-carrier protein ceruloplasmin would be low and copper will accumulate in the liver in unbound form -i.e. very reactive. That being said, with aging we tend to accumulate way more iron than copper, so the typical presentation is iron overload.

That's very interesting and makes sense, thank you.

 

[TNT]

It takes months and sometimes years for the thyroid to recover from poison vA. All vitamin E does is shove the vA into the liver so it makes it look like things are better, while filling up the liver with more toxic vA. When I was at my worst eating the typical Peat diet, I too was able to get relief from vA for a short bit by taking vitamin E. All it was doing was suppressing the symptoms by getting it out of the blood temporarily.

The gold standard from vA testing is a liver biopsy. Studies back in the 50's showed a third of the people tested via biopsy were vA toxic. Imagine now how high that percentage is with all the glyphosate and added and supplemented vA going around now.

Let me ask you this, Georgi. Why are more and more people able to get off their thyroid hormones after doing the low vA and low toxin diet? Does that not make you raise an eyebrow? Should we not be trying to get people off hormones instead of chaining them up for life? I absolutely believe thyroid hormones can and should be used as a crutch until full liver function comes back online but taking it for life is not a health solution, it sounds like captivity to me.

Have you checked out this twitter thread below by Dr. Smith?

View: https://twitter.com/NutriDetect/status/1594364556050313216


And lastly, throwing all studies aside. Results is what should really matter in the end. Grant healed stage 4 kidney disease! And results on the level that are happening in the low vA and low toxin groups are nothing short of miraculous. We all know we can find a study to suit our bias. However, if you are on the wrong bias you are going to get disastrous results like has been in the Ray Peat groups. There are people in the low vA groups literally calling Peat a murderer now because of how bad his diet recommendations harmed them. I do not agree with that kind of sentiment but the feelings are real for these people. They, like myself, were hurt badly by the Ray Peat way. Georgi, you yourself have been overweight for most this journey, wake up brother! I have lost almost 50 pounds not even trying! I feast like a king! A healthy diet should not make you fat! A healthy diet should not give you fatty liver like it did me or ecstatichamster, a healthy diet should not melt your teeth like it did me and Ray Peat himself.

@charlie , where are the low vitamin A groups?

 

[Sherbert]

“typical presentation is...high in iron/copper”

Does the slash mean, iron and copper, or, iron or copper? I ask coz ray would say say to up ones copper containing foods to keep out excess iron..

 

[Pete Rey]

I would suggest this video to understand it:

View: https://www.youtube.com/watch?v=JTdfRu_OFv0

Okay, I watched this and took notes. Let me just say it’s really hard to get through the snark and milking of the audience that would make Jack Kruse blush. Funny thing is, he knows how distasteful it is because he is constantly preempting objections he knows he’s going to get. “My business is information, I’m not giving it away for free.” Except you literally are right now. “Join the program because it’d be too much to go into here.” Come on bro, this is your 71st livestream. It’s one thing to have a membership for private content and personal consultation, but quit acting like a simple summary of what you do is proprietary IP that would wreck you if it got out.

Goading and salesmanship have no place in healing any more than they do in funeral parlors. It’s utterly laughable that he criticizes Ray’s morals when Ray was an absolute saint in this department. It’s just plain greed and hubris (endemic among doctors), and being born again doesn’t make it okay. He's like a walking definition of a Churchian. I would never give someone like this even a dollar on principle.

Anyway, that doesn't mean he's wrong. So on to the notes:

- Liver dumps the most toxic stuff that it doesn’t send to kidneys into bile
- Detox order: Liver to bile to feces (ideal), kidneys, skin
- Most health problems caused by too many toxins in the bile leading to cholestasis, both clinical and sub-clinical, both intrahepatic and extrahepatic, causing bile to leak into blood https://doi.org/10.1152/jappl.1970.29.6.806
- Cysts and tumors are the body’s last ditch attempt to “wall off” toxins from the bloodstream
- Copper is highly elevated in cancer tissue, ergo copper is toxic
- In gut dysbiosis, bacteria convert primary bile acids into secondary
- Secondary bile acids e.g. lithocholic acid are most toxic, known carcinogen
- Excess of lithocholic acid found in cysts: Bile Acids in Human Breast Cyst Fluid: The Identification of Lithocholic Acid*
- Low levels of bile found in blood, meaning no major liver/bile duct problems
- Yet there is no reason for any bile to be in blood unless it leaked, aka cholestasis
- “ Overall, biliary tract disease seems to be a distinct and important extrarenal complication of ADPKD” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5576944/
- Biliary tract disease = cholestasis = leaking bile
- ADPKD is genetic, theory is kidneys can’t get rid of bile fast enough, become cystic
- This causes a backlog in the detox order, causing the liver to then make cysts
- Liver and kidneys are filtering systems that feed both forwards and backwards
- Liver is first a filter, second a “sewage processing plant,” and third a storage depot
- Polycystic kidney disease + biliary dysgenesis appearing together in case study Polycystic kidney disease, biliary dysgenesis in a patient with Larsen's syndrome - PubMed
- Study on polycystic kidney diseases (dysgenesis = genetic bile duct malformations): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3953890/ (Smith comments italicized)
- “Despite improved survival, morbidity of this dual-organ disease (kidney + liver) is significant due to: a) renal collecting duct ectatic cysts and marked renal enlargement (i.e. storing something) leading to hypertension and progressive renal failure, and b) biliary dysgenesis leading to abnormal bile duct formation with progressive periportal congenital hepatic fibrosis (CHF). Patients with CHF develop portal hypertension with resulting esophageal or gastric varices (swollen varicose veins in the gut. Bile in stomach = acid reflux), enlarged hemorrhoids (also varicose veins), splenomegaly, hypersplenism, protein losing enteropathy and gastrointestinal bleeding (15).” In addition to CHF, non-obstructed dilation (not blocked, but getting bigger) of the intrahepatic bile ducts (Caroli’s syndrome) and dilation of the common bile duct occur in over 30% of ARPKD patients.”
- This is all to demonstrate that there is a connection between liver cysts and kidney diseases. Bile feeds forward to the kidneys. But if the kidneys can’t deal with it, bile builds up in blood, which feeds back into the liver, and the liver starts making “storage” cysts.
- “Choledochal cysts are congenital conditions involving cystic dilatation of bile ducts” (i.e. the cyst is pushing the bile duct open) Experiences of choledochal cyst in pediatric and adult... : Saudi Surgical Journal
- “Our results suggest that the PCK rat is a useful model for studies of biliary cystogenesis and treatment options of inherited cystic liver disease.” (bile is the connection) Biliary dysgenesis in the PCK rat, an orthologous model of autosomal recessive polycystic kidney disease - PubMed
- “High levels of bile acids in the colon may correlate with an increased risk of colon cancer, but the underlying mechanisms are not known.”Sulphation of lithocholic acid in the colon-carcinoma cell line CaCo-2 - PubMed
- High-fat diet also lowers bifidobacteria which is also linked to colon cancer and cholestasis
- Dysbiosis + bile dumping = lots of secondary bile acids in the gut
- SBAs damage the gut and cause cholestasis, get absorbed into the blood, and end up in cysts and tumors (shown in the breast cancer study)
- In sepsis, there is bile in the blood. “Resting serum bile acid concentrations were significantly higher in the septic group compared to the non-septic group combined.” Evaluation of Resting Serum Bile Acid Concentrations in Dogs with Sepsis
- Anthony Mawson says that vit A in the bile leaking into blood causes damage. Smith agrees but adds it’s just one problem of many, and built Toxic Bile Theory around that.

Makes sense to me. It's an impressive game of connect-the-dots, but the result seems like common sense. Bile going down/out = good; bile going up/in = bad. I don't see anything inherently anti-Peat in any of that minus the vit A and copper (which is nuanced). In fact I found this Peat quote posted by @Mauritio:

"Normally, our intestine and liver destroy most of the LPS endotoxin before it reaches the general circulation. The bile acids, a major end product of cholesterol, have a detergent action in the intestine that usually keeps endotoxin in solution, away from the absorptive surfaces of the intestine. If the flow of bile is obstructed, endotoxin is allowed to enter the system (Bertok, 2004). Estrogen can il"..hibit the flow of bile (Stieger, et aI., 2000). A mucus lining is part of the protective barrier, but the microscopic integrity of the intestinal cells themselves finally regulates the passage of materials into the blood and lymphatic vessels."
-RP

Looks to me like Peat was on this trail a long time before Smith.

So, I don't think he is a good person, I think he is resentful and a borderline predatory marketer, and if Genereux and Mawson are the genesis of the vitamin A story, and this is the crux of his contribution to their work, then I don't see the point in spending any more time on him. The debate should probably be focused on them.

 

[haidut]

“typical presentation is...high in iron/copper”

Does the slash mean, iron and copper, or, iron or copper? I ask coz ray would say say to up ones copper containing foods to keep out excess iron..

Usually iron, sometimes iron and copper, though the ratio is always in favor of iron (usually at least 5:1). Have not seen a case yet with only copper overload.

 

[Razvan]

You can see the "psycopath" behaviour of the low VA people. Speaking like a cult and preaching some kind of authority. Just reading those posts on twitter you can see that. This is what happens when eating too much beans and starch, it's going on for centuries and the "authority" is getting bigger just for the starch eating slaves to follow along.

 

[Peater]

@Pete Rey appreciate the effort you put into that post and your thoughts.

 

[Razvan]

Usually iron, sometimes iron and copper, though the ratio is always in favor of iron (usually at least 5:1). Have not seen a case yet with only copper overload.

Do you think k2 could raise ferritin? I have been getting the warming effect and circulation effect you should get from iron when you are anemic from it. I had anemia iron deficiency with low iron low ferritin and low hemoglobin from years of high dose aspirin, vitamin E and heavy dairy diet with almost no meat, i took iron for 1 month and hemoglobin is normal now, ferritin is in range but in the lower part. I stopped the iron and stopped the aspirin and E also. Iron raised things fast and easily, clearly showing that my iron stores were 0, but got some bad side effects from it, thats why I stopped when I saw the fast recovery of hemoglobin i had in just one month of supplementation.

 

[charlie]

Makes sense to me. It's an impressive game of connect-the-dots, but the result seems like common sense. Bile going down/out = good; bile going up/in = bad. I don't see anything inherently anti-Peat in any of that minus the vit A and copper (which is nuanced).

Thanks for the summary, very grateful! I just saw another amazing testimony in the groups, this kind of healing just cannot be overlooked. Something special is happening.

 

[haidut]

Do you think k2 could raise ferritin? I have been getting the warming effect and circulation effect you should get from iron when you are anemic from it. I had anemia iron deficiency with low iron low ferritin and low hemoglobin from years of high dose aspirin, vitamin E and heavy dairy diet with almost no meat, i took iron for 1 month and hemoglobin is normal now, ferritin is in range but in the lower part. I stopped the iron and stopped the aspirin and E also. Iron raised things fast and easily, clearly showing that my iron stores were 0, but got some bad side effects from it, thats why I stopped when I saw the fast recovery of hemoglobin i had in just one month of supplementation.

In general, ferritin rises either in response to increased iron intake (assuming the liver is not damaged) or as an acute biomarker of inflammation/infection. I have not seen much published data on vitamin K and ferritin, but it seems to raise RBC count (if low) in people taking higher doses (20mg+ daily) for things like osteoporosis. Heptadecanoic acid seems to be effective at regulating ferritin better, as described in the LipOdd thread.

LipOdd - Liquid Product With Odd-Chain Saturated Fats (SFA)

More than a decade ago, when I was just beginning my exploration of bioenergetics, one of the first indications that Ray's writings were onto something when it came to SFA vs. PUFA was the fact that while mainstream medicine ruthlessly bashed SFA in general and promoted PUFA, virtually very...

raypeatforum.com

 

[sunny]

In general, ferritin rises either in response to increased iron intake (assuming the liver is not damaged) or as an acute biomarker of inflammation/infection. I have not seen much published data on vitamin K and ferritin, but it seems to raise RBC count (if low) in people taking higher doses (20mg+ daily) for things like osteoporosis. Heptadecanoic acid seems to be effective at regulating ferritin better, as described in the LipOdd thread.

LipOdd - Liquid Product With Odd-Chain Saturated Fats (SFA)

More than a decade ago, when I was just beginning my exploration of bioenergetics, one of the first indications that Ray's writings were onto something when it came to SFA vs. PUFA was the fact that while mainstream medicine ruthlessly bashed SFA in general and promoted PUFA, virtually very...

raypeatforum.com

Did Dr. Peat ever say where he thought the ideal numbers were for serum iron and ferritin? He thought saturation % in the 20s was good.

 

[haidut]

Did Dr. Peat ever say where he thought the ideal numbers were for serum iron and ferritin? He thought saturation % in the 20s was good.

Serum iron by itself is almost meaningless. Ferritin, and iron saturation are much more important and I think he said they should all be in the bottom 20% of the range, with transferrin ideally being in the upper 20% of the range.